vacA Genotypes in Helicobacter pylori Strains Isolated from Children with and without Duodenal Ulcer in Brazil

Abstract

Data concerning the association between vacA genotypes and disease in children in both developed and developing countries are scarce, especially because of the small number of children with a duodenal ulcer studied. The vacA genotypes ofHelicobacter pylori strains obtained from 65 children (24 with a duodenal ulcer and 41 without a duodenal ulcer; 33 girls; mean age, 10.2 years; age range, 1 to 17 years) were investigated as described by J. C. Atherton et al. (J. Clin. Microbiol. 37:2979–2982, 1999). Ten (15.4%) children were infected with more than one H. pylori strain. None of these patients were included in our analysis of the relationship between gastric disorders and specific vacA genotypes. The s1 allele was detected in all H. pylori strains isolated from patients with a duodenal ulcer and from 21 (58.3%) patients without a duodenal ulcer (P = 0.003). Strains with the s2 allele were found only in patients without ulcer (n = 15; 41.7%). Most s1 strains had the s1b allele (97.5%), a result similar to that reported for adults from the Iberian peninsula, which could reflect the Brazilian population origin. One untypeable s1 strain was isolated. The m1 allele was also more frequently found in strains obtained from duodenal ulcer patients (P= 0.028). The m2 allele was found in strains obtained from 20 (36.4%) children, 3 (15.8%) with an ulcer and 17 (47.2%) without an ulcer. Only one m hybrid strain (m1 and m2 hybrid) was detected. It was demonstrated for the first time that the frequencies of colonization with strains with the s1 allele (14.3% in children up to 8 years of age and 85.7% in older patients;P = 0.012) and of strains with the m1 allele (11.1% in patients up to the age 8 years and 88.9% in older children;P = 0.013) increase with age.

The transmission of Helicobacter pylori from stomach to stomach

“…The evidence from the geographical distribution of alleles of the gene for the vacuolating cytotoxin vacA (see below) supports this. The predominance of the s1b allele in the Iberian peninsula and South America is consistent with the historically recognized spread of persons from Southern Europe to South America, and it has been suggested that the s1b allele was carried to the American continent by early explorers and that Helicobacter was introduced into this population only about 500 years ago 2 . On the other hand, evidence for the presence of Helicobacter in pre‐Columbian human remains has been presented.…”

The association of vacA genotype and Helicobacter pylori-related disease in Latin American and African populations

“…Recently, several studies have consistently shown that the vacA genotype is associated with disease in patients from various countries [18][19][20]25,32,33,36,38,49,51]. However, most of the articles investigating H. pylori strains from Latin America and Africa have shown no significant relationship between vacA genotypes and gastrointestinal diseases ( Table 1).…”

“…The vacA s1 genotype was linked to an increased risk of gastric cancer in four of the eight (50.0%) studies [25,33,49,51], and this genotype was also linked to an increased risk of peptic ulcers in five of 19 (26.3%) studies [32,33,36,38,49]. Likewise, the m1 genotype was linked to gastric cancer in three of six (50.0%) studies [25,33,49] and to peptic ulcers in four of 17 (23.5%) studies [32,33,38,49]. In Latin America, the frequency of the vacA s1 genotypes and s1m1 combination genotype in strains isolated from peptic ulcer or gastric cancer patients was significantly higher than from those with gastritis alone (Table 4).…”

A New Model for the Transmission ofHelicobacter pylori: Role of Environmental Reservoirs as Gene Pools to Increase Strain Diversity

“…Recent evidence has also showed that multiple H. pylori strains and other Helicobacter spp. are able to infect simultaneously the GI tract of one individual (Van den Bulck et al 2005;Fritz et al 2006;De Gusmao et al 2000;Daugule et al 2003;Ghose et al 2005;Kang and Blaser 2006;Israel et al 2001). Even in cases where multiple strains may occur as a result of intensive genetic recombination of a single ancestral strain, it is recognized that the ancestor had to be in contact with other strains (Delport et al 2006).…”